This invention relates to method and apparatus for guided ablative therapy and more particularly to such therapy to treat fast ventricular arrhythmia.
The electrical activity generated in certain organs in the human body is intimately related to the organs' functions. Abnormalities in cardiac and brain electrical conduction processes are principal causes of morbidity and mortality in the developed world. Appropriate treatment of disorders arising from such abnormalities frequently requires a determination of their location. Such localization of the site of origin of an abnormal electrical excitation is typically achieved by painstaking mapping of the electrical activity on the inner surface of the heart or the brain from electrodes or a catheter. Often, this recording must be done while the abnormal biological electrical excitation is ongoing.
Radio frequency catheter ablation procedures have evolved in recent years to become an established treatment for patients with a variety of supraventricular [Lee, 1991; Langberg, 1993] and ventricular arrhythmias [Stevenson, 1997; Stevenson, 1998]. However, in contrast to supraventricular tachycardia ablation, which is highly successful because the atrio-ventricular node anatomy is known, ventricular tachycardia ablation remains difficult because the site of origin of the arrhythmia could be anywhere in the ventricles.
Sustained ventricular tachycardia is often a difficult arrhythmia to manage. One of the most common indications for radio frequency catheter ablation of ventricular tachycardia is arrhythmia refractory to drug therapy that results in frequent discharges from an implantable cardioverter-defibrillator. Radio frequency ablation is also indicated when the ventricular tachycardia is too slow to be detected by the implantable cardioverter-defibrillator or is incessant [Strickberger, 1997].
Selection of the appropriate target sites for ablation is usually based on a combination of anatomical and electrical criteria. The ability of the physician to deliver radio-frequency energy through a catheter at the reentry site is restricted by the limitations of the current technology that is employed to guide the catheter to the appropriate ablation site. The principal limitation of the radio frequency ablation technique is the determination of the correct site for delivery of the radio frequency energy. Conventionally, this determination is achieved by painstaking mapping of the electrical activity on the inner surface of the heart from electrodes on the catheter. Often, this recording must be done while the arrhythmia is ongoing. This is a major problem, especially for those arrhythmias which compromise hemodynamic function of the patient. Many arrhythmias for this reason are not presently amenable to radio frequency ablation treatment.
The acute lesion created by radio frequency current consists of a central zone of coagulation necrosis surrounded by a zone of hemorrhage and inflammation. Arrhythmias may recur if the target tissue is in the border zone of a lesion instead of in the central area of necrosis. If the inflammation resolves without residual necrosis, arrhythmias may recur several days to several weeks after an apparently successful ablation [Langberg, 1992]. Conversely, an arrhythmia site of origin that was not initially successfully ablated may later become permanently nonfunctional if it lies within the border zone of a lesion and if microvascular injury and inflammation within this zone result in progressive necrosis [Nath, 1994]. Thus, the efficacy and long term outcome of catheter ablation depend on accurate determination of the site of origin of the arrhythmia.
Catheter ablation of sustained monomorphic ventricular tachycardia late after myocardial infarction has been challenging. These arrhythmias arise from reentry circuits that can be large and complex, with broad paths and narrow isthmuses, and that may traverse subendocardial, intramural, and epicardial regions of the myocardium [deBakker, 1991; Kaltenbrunner, 1991]. Mapping and ablation are further complicated by the frequent presence of multiple reentry circuits, giving rise to several morphologically different ventricular tachycardias [Wilbur, 1987; Waspel, 1985]. In some cases, different reentry circuits form in the same abnormal region. In other cases, reentry circuits form at disparate sites in the infarct area. The presence of multiple morphologies of inducible or spontaneous ventricular tachycardia has been associated with antiarrhythmic drug inefficacy [Mitrani, 1993] and failure of surgical ablation [Miller, 1984].
Several investigators have reported series of studies of patients selected for having one predominant morphology of ventricular tachycardia (“clinical ventricular tachycardia”) who were treated with radio frequency catheter ablation [Morady, 1993; Kim, 1994]. It is likely that this group of patients represents less than 10% of the total population of patients with ventricular tachycardia [Kim, 1994]. The patient must remain hemodynamically stable while the arrhythmia is induced and maintained during mapping. The mapping procedure may take many hours during which the arrhythmia must be maintained. Thus, currently, radio frequency catheter ablation is generally limited to “slow” ventricular tachycardia (about 130 bpm) which is most likely to be hemodynamically stable.
Ablation directed towards the “clinical tachycardia” that did not target other inducible ventricular tachycardias successfully abolished the “clinical ventricular tachycardia” in 71% to 76% cases. However, during follow-up up to 31% of those patients with successful ablation of the “clinical ventricular tachycardia” had arrhythmic recurrences, some of which were due to different ventricular tachycardia morphologies from that initially targeted for ablation.
Furthermore, there are several difficulties in selecting a dominant, “clinical ventricular tachycardia” for ablation. Often it is not possible to determine which ventricular tachycardia is in fact the one that has occurred spontaneously. In most cases, only a limited recording of one or a few ECG leads may be available. In patients with implantable defibrillators ventricular tachycardia is typically terminated by the device before an ECG is obtained. Even if one ventricular tachycardia is identified as predominant, other ventricular tachycardias that are inducible may subsequently occur spontaneously. An alternative approach is not to consider the number of ventricular tachycardia morphologies in determining eligibility for catheter ablation but rather to attempt ablation of all inducible ventricular tachycardias that are sufficiently tolerated to allow mapping [Stevenson, 1998b; Stevenson, 1997]. However, this approach requires that the patient be hemodynamically stable during the ventricular tachycardia mapping procedure.
The use of fluoroscopy (digital bi-plane x-ray) for the guidance of the ablation catheter for the delivery of the curative radio frequency energy is common to clinical catheter ablation strategies. However, the use of fluoroscopy for these purposes may be problematic for the following reasons: (1) It may not be possible to accurately associate intracardiac electrograms with their precise location within the heart; (2) The endocardial surface is not visible using fluoroscopy, and the target sites can only be approximated by their relationship with nearby structures such as ribs and blood vessels as well as the position of other catheters; (3) Due to the limitations of two-dimensional fluoroscopy, navigation is frequently inexact, time consuming, and requires multiple views to estimate the three-dimensional location of the catheter; (4) It may not be possible to accurately return the catheter precisely to a previously mapped site; (5) It is desirable to minimize exposure of the patient and medical personnel to radiation; and (6) Most importantly, fluoroscopy cannot identify the site of origin of an arrhythmia and thus cannot be used to specifically direct a catheter to that site.
Electro-anatomic mapping systems (e.g., Carto, Biosense, Marlton, N.J.) provide an electro-anatomical map of the heart. This method of nonfluoroscopic catheter mapping is based on an activation sequence to track and localize the tip of the mapping catheter by magnetic localization in conjunction with electrical activity recorded by the catheter. This approach has been used in ventricular tachycardia [Nademanee, 1998; Stevenson, 1998], atrial flutter [Shah, 1997; Nakagawa, 1998], and atrial tachycardia ablation [Natale, 1998; Kottkamp, 1997]. The ability to localize in space the tip of the catheter while simultaneously measuring the electrical activity may facilitate the mapping process. However, this technique fundamentally has the limitation that it involves sequentially sampling endocardial sites. The mapping process is prolonged while the patients must be maintained in ventricular tachycardia. Also, the localization is limited to the endocardial surface and thus sites of origin within the myocardium cannot be accurately localized.
The basket catheter technique employs a non-contact 64-electrode basket catheter (Endocardial Solutions Inc., St. Paul, Minn.) placed inside the heart to electrically map the heart. In the first part of this procedure high frequency current pulses are applied to a standard catheter used in an ablation procedure. The tip of this catheter is dragged over the endocardial surface, and a basket catheter is used to locate the tip of the ablation catheter and thus to trace and reconstruct the endocardial surface of the ventricular chamber. Then the chamber geometry, the known locations of the basket catheter, and the non-contact potential at each electrode on the basket catheter are combined in solving Laplace's equation, and electrograms on the endocardial surface are computed. This technique has been used in mapping atrial and ventricular arrhythmias [Schilling, 1998; Gomick, 1999]. One of the drawbacks of this methodology is that the ventricular geometry is not fixed but varies during the cardiac cycle. In addition, the relative movement between the constantly contracting heart and the electrodes affects the mapping. While the inter-electrode distances on each sidearm of the basket catheter are fixed, the distances between the actual recording sites on the endocardium decrease during systole. This leads to relative movement between the recording electrode and the tissue, significantly limiting the accuracy of the mapping method. Also, the localization is limited to the endocardial surface, and thus sites of origin within the myocardium cannot be accurately localized.
U.S. Pat. Nos. 6,308,093 and 6,370,412, the contents of which are incorporated herein by reference, present a method in which a single equivalent moving dipole (SEMD) model can be used to localize an electrical source within the body. One of the co-inventors of the present application is a co-inventor of these two patents. The concept of considering the heart as a single dipole generator originated with Einthoven [Einthoven, 1912], and its mathematical basis was established by Gabor and Nelson [Gabor, 1954]. Several investigators [Mirvis, 1981; Gulrajani, 1984], [Tsunakawa, 1987] have studied the cardiac dipole in clinical practice and attempted to determine the dipolar nature of the ECG. The advantages of the use of the equivalent cardiac dipole are: (1) It permits quantification of source strength in biophysical terms that are independent of volume conductor size (classic electrocardiography), and (2) The active equivalent source can be localized and assigned a location, something that cannot be done using classical electrocardiography.
For many arrhythmias, the electrical activity within the heart is highly localized for a portion of the cardiac cycle. During the remainder of the cardiac cycle the electrical activity may become more diffuse as the waves of electrical activity spread. It is not possible to construct the three-dimensional distribution of cardiac electrical sources from a two-dimensional distribution of ECG signals obtained on the body surface. However, if it is known that a source is localized, then this localized source can be approximated as a single equivalent moving dipole (SEMD), for which one can compute the dipole parameters (i.e., location and moments) by processing electrocardiographic signals acquired from recording electrodes placed on the body surface or in the body.
As described in U.S. Pat. Nos. 6,308,093 and 6,370,412, fitting the dipole parameters to body surface ECG signals provides a solution for the dipole location as well as for its strength and orientation (referred to herein as the “Inverse Dipole Method”). The location of the dipole at the time epoch when the electrical activity is confined to the vicinity of the site of origin of an arrhythmia should coincide with the site of origin of the arrhythmia. In contrast to standard mapping techniques, the inverse solution can be computed from only a few beats of the arrhythmia, thereby eliminating the need for prolonged maintenance of the arrhythmia during the localization process.
In previous methods [Armoundas, 1999; Armoundas, 2001; Armoundas, 2003] after the site of origin of the arrhythmia is localized, one or more electrodes at the ablation catheter tip are used to deliver low-amplitude (sub-threshold) bipolar current pulses, and the resulting signals are recorded and processed to locate the position of the catheter tip dipole using the same Inverse Dipole Method. The catheter tip is guided towards the site of origin of the arrhythmia using the relative calculated locations of the respective dipoles. When the catheter tip dipole and arrhythmic site dipole are calculated to have nearly identical locations, the location of the actual catheter tip should also nearly coincide with the site of origin of the arrhythmia. Ablative energy is then delivered. This method of source localization and catheter guidance shall be referred to herein as the “Inverse Dipole Method”.
When the rate of the ventricular tachycardia is low, the electrical activity from the previous cardiac cycle is no longer present when the next cardiac cycle begins. On the other hand, if the ventricular tachycardia is fast, electrical activity from the previous cycle, now for the most part remote from the site of origin of the arrhythmia, is still present when the next wave of depolarization emerges from that site. The bioelectric source dipole is computed from the body surface potentials which in turn reflect a summation of all on-going electrical activity in the heart. At the start of the QRS complex during fast ventricular tachycardia the bioelectrical source dipole will be a summation of both the remote electrical activity associated with the previous cardiac cycle and the localized activity newly emerging from the site of origin of the arrhythmia. Consequently, the location of the bioelectric source dipole will no longer correspond to the location of the site of origin of the arrhythmia. Therefore, even if the catheter tip and site of origin of the arrhythmia are in reality superposed, the previously described method will identify their locations as being different. It is clear that the method described previously for localizing the arrhythmic site dipole will work only in the context of slow ventricular tachycardia.
What is needed is a means of efficiently directing the tip of a catheter to the site of origin of both slow and fast arrhythmias to allow the Inverse Dipole Method to be used in all contexts.